Thermal, ventilatory, and gluco-regulatory responses during exercise following short-term acetylsalicylic acid ingestion

Acetylsalicylic acid and exercise combined produce perturbations in thermal, respiratory and carbohydrate metabolism. However, the therapeutic implications of these therapies are antithrombotic and fibrinolytic respectively. In a double-blind, counterbalanced cross-over design of eight men, salicylate ingestion in combination with 60 min of moderate intensity exercise (50% VO2 max) significantly increased respiratory rate and oxygen consumption (p less than 0.05) both at rest and during the exercise protocol. The effect of acetylsalicylic acid ingestion on gluco-regulatory and counter-regulatory hormones was not significant compared to the placebo. These data suggest a safe prophylactic role for a combined short-term acetylsalicylic acid ingestion and exercise therapy in the development of coronary artery disease when exercising in a thermal neutral environment.     

肺脏超声对新生儿呼吸窘迫综合征的诊断研究

目的 研究肺脏超声对新生儿呼吸窘迫综合征(RDS)的诊断价值.方法 2015年4月至2016年10月,对在本院新生儿科住院经临床、动脉血气分析和胸部x线检查确诊为RDS、同时行肺部超声检查的50例患儿为研究组,同期住院的50例非肺病患儿为对照组.在安静状态下,患儿取仰卧、侧卧或俯卧位,以腋前线、腋中线、腋后线为界,将肺脏分成前、侧、后3个区域,探头与肋骨垂直分别对双侧肺脏的每个区域进行扫查,并与传统胸部x线检查结果作对照.结果 (1)肺实变、胸膜线异常、肺泡-间质综合征等征象在本组所有RDS患儿均存在(1 00％),而在正常对照组均不存在(0％)(P＜0.05);A-线消失在RDS为86％、对照组为0％(P＜0.05);肺滑消失与肺搏动在RDS患儿的发现率为52％、而对照组为0％(P＜0.05).(2)不同肺野超声征象的不一致性:不但双侧肺脏的超声表现可以不同,即使同一侧肺脏不同肺野的超声征象也可不一致.(3)动态观察:治疗后,随病情恢复,可见肺实变范围逐渐缩小、肺泡-间质综合征减轻、胸膜线恢复正常及A-线逐渐出现等.结论 实变、胸膜线异常与肺泡-间质综合征是RDS的主要超声影像学表现,其中,肺实变是超声诊断RDS的必备征象.超声诊断RDS准确可靠,敏感性高、特异性强,且具有简便、无创、可在床边开展、可随时检测、可避免射线损伤等优点.     

Paraquat

The herbicide paraquat has claimed many fatalities due to accidental or deliberate ingestion of the concentrated form of the substance. Unlike most other poisons, the clinical course of paraquat intoxication is often protracted, and there is no known antidote for it. Treatment is often unsatisfactory. The principal target for the poison is the lung. Here, it causes destruction of the alveolar epithelium, followed by a progressive, inexorable, pulmonary fibrosis which causes death from respiratory failure. The pulmonary fibrosis starts with an infiltration into the alveolar spaces of primitive fibroblasts (profibroblasts) which differentiate into mature cells that completely occlude the alveolar spaces. Small quantities of collagen are also produced. The result is a cellular intra-alveolar fibrosis. Paraquat lung is not, therefore, a kind of diffuse interstitial pulmonary fibrosis as was once believed. The mechanism by which paraquat produces its toxic effects is obscure. It has a destructive action on epithelia, and in the lung, this may be enhanced by the high oxygen tension there. There is no satisfactory explanation for its fibrogenic action although this process may be aggravated by oxygen therapy. Even after 10 years, treatment for paraquat poisoning consists mainly of removing the paraquat from the stomach with colloidal material (bentonite) and from the blood with forced diuresis and/or hemodialysis. Steroid therapy has produced little success in halting the fibrosis, but better results are claimed from immunosuppressive and cytotoxic drugs. Recent research indicates that superoxide dismutase may be more successful as an antidote.     

Two cases of organophosphate poisoning with development of intermediate syndrome

Two cases of intermediate syndrome caused by organophosphorus poisoning are reported. Trichlorfon, propoxur (a carbamate pesticide) and fenthion were ingested in both attempts at suicide. After successful conventional therapy during the cholinergic phase, but before the time when the onset of delayed neuropathy might be expected, an intermediate syndrome developed. It affected the proximal limb muscles, neck flexors and respiratory muscles 2 d after pesticide ingestion. The two patients needed respiratory support. Recovery from the intermediate syndrome was complete in both patients, although one subsequently developed delayed neuropathy.     

Angioedema complicating lisinopril therapy.

A case of angioedema induced by antihypertensive therapy with lisinopril is presented. The patient was a 70 year old black woman, with a history of hypertension for 15 years. The patient presented with acute onset of swelling involving the oro-facial region and respiratory distress after ingestion of three doses of lisinopril over a three day period. A clinical diagnosis of drug induced angioedema was made based on clinical presentation. The patient was treated with diphenhydramine, 50 mg intravenously, and hydrocortisone 100 mg every eight hours with resolution of her symptoms over a 24 hour period. Angioedema should be recognized as a possible life threatening complication of therapy with lisinopril, and other angiotensin converting enzyme (ACE) inhibitors. This usually responds to therapy with antihistamines and steroids if recognized early.     

间质性肺疾病合并呼吸衰竭相关因素及机械通气治疗价值

目的分析间质性肺疾病(ILD)合并呼吸衰竭的相关因素,并探讨机械通气的治疗价值。方法回顾性分析我院自2006年6月至2011年6月收治的间质性肺疾病合并呼吸衰竭应用机械通气治疗的42例患者的临床资料。结果呼吸衰竭相关因素有ILD急性加重,呼吸道感染,肺栓塞,心力衰竭;急性期7d、14d、30d的生存率依次为97.6%、92.9%、83.3%。有创机械通气病死率88.33%,无创机械通气病死率56.67%,两组组间差异显著,P<0.05。住院总病死率64.28%。结论呼吸道感染、ILD急性加重、肺栓塞及合并心力衰竭是呼吸衰竭相关因素,无创通气治疗效果优于有创通气。     

Butanol ingestion in an airport hangar

1-Butanol is a colourless organic solvent with a rancid sweet odour. 1-Butanol ingestion may result in vomiting, abdominal pain, headache, drowsiness and unconsciousness. We present a 47-year-old male with no previous medical history, who was found comatose and soiled after having vomited while unconscious. On arrival, he had a Glasgow coma scale of 3, tachycardia, hypotension, shallow tachypnoic breathing, hypotonic muscles, absent myotatic reflexes and aromatic odour. The patient was intubated and treated with oxygen, dopamine and volume replacement therapy. Gastric lavage was performed and activated charcoal was given. His initial laboratory test revealed hypokaliemia, renal failure, acidosis with elevated lactate and hypercapnic respiratory insufficiency. Twelve hours after admission, the patient started to respond to a painful stimulus and 4 h later he was conscious. He was extubated 23 h after admission. All pathological laboratory results gradually returned within normal limits. The subsequent toxicological examination of gastric content and urine sample by gas chromatography revealed 1-butanol. On awakening, he confirmed ingestion of a solvent stored in an airport hangar. In conclusion, we describe a patient who ingested - a posteriori with suicidal intention - an unknown dose of 1-butanol. Symptoms were headache, vomiting, abdominal pain, coma, muscular hypotonus, hypotension, respiratory insufficiency and mixed acidosis. The patient totally recovered after supportive therapy over 30 h. In future cases, intravenous administration of ethanol or even hemodialysis can be considered analogous to the treatment of methanol and ethylene glycol poisoning.     

Cigarette smoking and diffuse lung disease

Cigarette smoke, a toxic collection of more than 4000 chemicals generated from combustion of tobacco plant leaves, is known to cause several respiratory ailments, including chronic bronchitis, emphysema and lung cancer, and is associated with an increase in respiratory infections. In addition, cigarette smoking is considered a principal aetiological factor responsible for the development of certain diffuse interstitial and bronchiolar lung diseases, namely respiratory bronchiolitis-interstitial lung disease (RB-ILD), desquamative interstitial pneumonia (DIP) and adult pulmonary Langerhans' cell histiocytosis (PLCH). Although not exclusively seen in cigarette smokers, substantial clinical and epidemiological data support a central role for smoking as the primary causative agent of most RB-ILD, DIP and PLCH. Additional evidence in support of cigarette smoke as a primary aetiological agent in RB-ILD, DIP and PLCH is the observation that smoking cessation may lead to disease improvement, while recurrence of these disorders has been observed to occur in the transplanted lung upon re-exposure to tobacco smoke. Furthermore, histopathological changes of respiratory bronchiolitis, DIP and PLCH (with or without co-existent emphysema) may be found on lung biopsy in the same individual, implicating smoking as a common inciting agent of these diverse lesions. Recent studies also suggest a role for cigarette smoking as a potential co-factor in the development of acute eosinophilic pneumonia, usual interstitial pneumonia and rheumatoid arthritis-associated interstitial lung disease. In the current review, we propose a novel classification that takes into account the complex relationship between cigarette smoking and diffuse lung diseases. Investigation on the role of smoking as a potential causative factor or modifier of these diverse diffuse lung diseases is important, as smoking cessation utilizing state-of-the-art tobacco cessation efforts should be a central part of therapy, while pharmacotherapy with corticosteroids or other immune modifying agents should be reserved for selected patients.     

Delayed immunosuppressive treatment in life-threatening paraquat ingestion: A case report

Introduction

Combined glucocorticoids and cyclophosphamide pulse therapy showed promising results in moderate-to-severe paraquat poisonings to reduce life-threatening respiratory complications. Its benefit has been observed when given early in the course of poisoning; however, whether its delayed administration remains beneficial is unknown.

Case Report

We describe a 23-year-old male who ingested 70 mL of a commercialized concentrate formulation with 20% weight/volume paraquat in a suicide attempt. Within 24 hours from paraquat ingestion, he presented most of the indicators of poor outcome, including gastritis, early renal dysfunction, dark blue urine colorimetric dithionite test, and marked plasma paraquat concentrations (0.56 μg/mL at 13 hours, and 0.41 μg/mL at 24 hours after ingestion). The patient received early gastrointestinal decontamination and aggressive supportive treatments. However, due to a rapidly progressive severe pulmonary infection, glucocorticoids and cyclophosphamide were delayed until day 14. Interestingly, our patient survived with mild respiratory sequelae despite poor initial prognosis.

Discussion

This observation suggests the potential benefit of immunosuppressive pulse therapy, even if administered 14 days after paraquat ingestion, and highlights the role of paraquat-induced alveolitis in the development of fibrosis.

Conclusion

Combined glucocorticoids and cyclophosphamide should be considered in moderate-to-severe paraquat poisonings, even if delayed.     

Myocardial lysis in a fetus induced by maternal paraphenylenediamine poisoning following an intentional ingestion to induce abortion

The acute toxicity of paraphenylenediamine (PPD) has been associated with several histopathological changes. In humans, acute PPD poisoning is known to cause rhabdomyolisis and particularly myocardial lysis. However, its toxicity for the fetus has never been reported in the literature. We report a case of myocardial lysis in a fetus expelled by a 22-year-old mother after apparent ingestion of an unknown amount of PPD. The patient was admitted to our intensive care unit with acute onset of respiratory distress and rhabdomyolysis. The pelvic ultrasonography on admission showed a normally progressing pregnancy of 23-24 weeks. On day 9 post-ingestion, the patient spontaneously expelled a non-viable fetus. The fetal examination did not show any external or macroscopic abnormalities. However, the histopathological exam showed an important heart and lung congestion. There was also some interstitial edema and inflammation at the base of the lingua, in addition to a chorionic villus thrombosis and abruptio placentae. The histopathology of the myocardium showed lysis of the cardiac muscle. This observation suggests that the PPD was most likely responsible for the myocardial injury in the fetus.     

Fetal poisoning after maternal paraquat ingestion during third trimester of pregnancy: Case report and literature review

Introduction

Paraquat remains one of the common substances involved in intentional ingestions in Thailand. However, data on outcomes of paraquat ingestion during pregnancy is rarely available and the management is controversial.

Case report

A 17-year-old female in 36+ weeks of gestation attempted suicide by ingesting 1/2 a glass of Gramozone? (paraquat 27.6 % w/v) 5 hours prior to arrival to the hospital. Gastric aspiration and lavage was performed and she was given 50 g of activated charcoal and 150g of Fuller’s Earth suspension. A male infant, weighing 2,390g with an Apgar score of 7¹ 10¹⁰, was delivered via emergency caesarean section 7 hours after ingestion. Due to presence of paraquat in the gastric lavage fluid, the mother was placed on dexamethasone/cyclophosphamide therapy. She developed mild renal insufficiency 63 hours after the ingestion. The infant developed tachypnea immediately after birth that self-resolved. The infant developed tachypnea again on day 6 of life. A chest x-ray revealed right lower lobe infiltration that progressed to diffuse interstitial pattern; subsequent chest x-rays showed evidence of fibrosis. Both mother and infant survived and the infant was discharged and sent home with oxygen 0.5 LPM. Upon follow up at 10 months of age, he still had evidence of chronic lung disease clinically and on chest x-ray.

Conclusion

Paraquat ingestion during the third trimester of pregnancy usually carries a very poor prognosis. Review of reported literature suggests that this case report represents only the second survival of mother and child.     

Acute tetrachloroethylene poisoning--blood elimination kinetics during hyperventilation therapy

After ingestion of 12-16 g tetrachloroethylene, a 6-year-old boy was admitted to the clinic in coma. In view of the high initial tetrachloroethylene blood level, hyperventilation therapy was performed. Under this therapeutic regimen, the clinical condition of the patient improved considerably. The tetrachloroethylene blood level profile which was determined under hyperventilation therapy could be computer-fitted to a two-compartment model. Elimination of tetrachloroethylene from the blood compartment occurred via a rapid and a slow process with half-lives of 30 min and 36 hours, respectively. These values compared favourably with the half-lives of 160 min and 33 hours under normal respiratory conditions. During hyperventilation therapy, the relative contribution to the fast elimination process increased from 70% for physiological minute volume to 99.9%. A minor fraction of the ingested dose was excreted with the urine (integral of 1% during the first 3 days). In contrast to previous results, trace amounts of unchanged tetrachloroethylene were detected in the urine besides trichloroacetic acid and trichloroethanol.     

原发性干燥综合征相关急进性肺间质病变（1例报告并文献复习）

目的提高对原发性干燥综合征相关急进性肺间质病变临床特征认识。方法结合1例原发性干燥综合征相关性肺间质病变临床资料进行文献复习。结果患者,女,62岁,因咳嗽气喘5 d入院,诊断：①急进性肺间质病变,呼吸衰竭。②原发性干燥综合征。强的松治疗有效。结论原发性干燥综合征相关急进性肺间质病变是一种少见严重并发症,胸部HRCT对急进性肺间质病变诊断和疗效评估起重要作用。早期诊断,积极免疫抑制治疗能改善预后。     

Respiratory Failure Following Isolated Ziprasidone Ingestion in a Toddler

Ziprasidone is an atypical antipsychotic approved for the treatment of schizophrenia and bipolar mania in adults and is used off label in children and adolescents. Despite increasing use of ziprasidone in both adult and pediatric populations, there remains a paucity of reports describing unintentional pediatric exposures. The following report describes a patient with isolated ziprasidone ingestion who required intubation secondary to respiratory failure. A 15-month-old previously healthy boy presented to the emergency department shortly after his father found him with approximately five partially dissolved 80-mg ziprasidone tablets in his mouth. The child was flaccid and lethargic with no eye opening, withdrawing from pain only. Two hours after arrival, he developed worsening CNS depression with inability to protect his airway and underwent endotracheal intubation. A serum ziprasidone level was 330 ng/mL by LC/MS. The patient was extubated approximately 14 h later and was discharged from the hospital shortly thereafter in good health without neurological sequelae. Isolated pediatric ingestion of ziprasidone resulting in the need for significant medical intervention has not been previously reported. We report a case of respiratory failure requiring intubation following accidental ziprasidone ingestion with confirmatory serum levels.     

Interstitial Pneumonitis from Treatment with Gemcitabine

Introduction:

The use of gemcitabine may lead to numerous adverse effects ranging from mild to very severe, such as interstitial pneumonitis. The diagnosis of this complication is based on multiple laboratory findings, radiographic evidence, and high clinical suspicion. Presented is a case report of a patient who met these criteria and had onset consistent with drug-induced interstitial pneumonitis.

Case Presentation:

A 76-year-old White female was treated with gemcitabine for pancreatic cancer. Two months after the initiation of therapy, she was admitted to the hospital for worsening dyspnea and cough. High clinical suspicion, bilateral interstitial opacities on chest x-ray, worsening pulmonary status, and onset 2 months after initiation of therapy led to the diagnosis of gemcitabine-induced interstitial pneumonitis. Steroid therapy with prednisone was initiated, and the patient’s clinical symptoms and radiographic findings improved.

Discussion:

Gemcitabine-induced interstitial pneumonitis is well described in the literature. It is a rare but serious complication associated with gemcitabine therapy in which patients present with worsening dyspnea. Most patients only require supportive care and discontinuation of the drug for treatment, but in severe cases supplemental oxygen and steroid therapy must be used before resolution of symptoms. It is important to obtain an accurate medication history to evaluate for other potentially pulmonary toxic medications. Radiographic findings such as bilateral infiltrates should be completely resolved after therapy.

Conclusion:

Radiographic findings, clinical symptoms, and clinical suspicion can lead to early recognition of interstitial pneumonitis from gemcitabine. Physician awareness of this adverse effect and early recognition are keys to providing prompt treatment in resolving symptoms and decreasing mortality.Key Words: gemcitabine, pneumonitis, pulmonary toxicityGemcitabine is an antineoplastic agent used for the treatment of cancers such as non-small-cell lung and pancreatic cancer. Antineoplastic agents are vital to patient outcomes due to the high mortality rate of untreated forms of cancer. Gemcitabine is a pyrimidine antimetabolite that inhibits DNA synthesis thus affecting many organ systems. Common adverse events include myelosuppression, dyspnea, nausea, and vomiting. The severity and duration of dyspnea vary based on individual factors. A severe form of lung toxicity associated with gemcitabine is known as interstitial pneumonitis, which involves acute or chronic interstitial fibrosis of the lung with the tissues becoming stiff and scarred. The fibrosis of the lung interferes with the patient’s ability to breathe. The incidence of interstitial pneumonitis from gemcitabine is estimated at 1% to 2% when the drug is used as a single agent in treatment.¹ The incidence may increase when combined with other agents potentially associated with pulmonary toxicity and should be treated early to improve chances of recovery. Underlying pulmonary dysfunction increases the risk of gemcitabine-induced pulmonary toxicity. ²The exact mechanism of lung toxicity remains unknown; however, proposed mechanisms have been documented in the literature. One proposed mechanism of toxicity is the release of cytokines in the body, which could result in damage to areas throughout the body. This process could lead to capillary leak syndrome or pulmonary edema. ³The diagnosis of interstitial pneumonitis is difficult due to the multiple etiologies of lung dysfunction and should include other likely diagnoses consistent with bilateral interstitial opacities on chest x-ray and worsening respiratory status. Myelosuppression, a common and well-documented adverse event with gemcitabine use, increases the likelihood of acquiring an infection that could decrease lung function. ⁴This article follows a patient who presented with increased cough and dyspnea that progressed to respiratory failure. The patient was diagnosed with interstitial pneumonitis likely secondary to gemcitabine. This case report follows the progression of the illness, the treatment, and her response to treatment.     

Fatal interstitial pneumonitis in a patient with relapsed diffuse large B cell lymphoma following yttrium-90 ibritumomab tiuxetan

There is no previous report of fatal interstitial pneumonitis related to the administration of yttirum-90 ibritumomab tiuxetan. We report first case of fatal interstitial pneumonitis in a 35-year-old female patient with relapsed diffuse large B cell lymphoma following yttrium-90 ibritumomab tiuxetan. A pathological evaluation through a surgical lung biopsy demonstrated a “interstitial pneumonitis” pattern. Although high-dose methylprednisolone was administered, she died due to acute respiratory distress syndrome, secondary to radioimmunotherapy-induced interstitial pneumonitis. In this report, we discuss the etiology, diagnosis, and management of radioimmunotherapy-induced interstitial pneumonitis.     

结缔组织病肺间质病变临床分析

目的提高对结缔组织病肺间质病变的认识及诊断。方法回顾性分析124例结缔组织病肺间质病变患者呼吸系统的临床表现、肺功能检查、肺部影像学特点、有无肺动脉高压、肺功能与肺部影像学关系。结果124例结缔组织病肺间质病变患者呼吸系统临床表现为咳嗽、咳痰、气短、胸闷憋气,严重时表现为活动耐量下降、呼吸困难。64例行肺功能检查均有弥散功能减低,其中26例为单纯弥散功能减低,32例为限制性通气功能障碍伴弥散功能减低,4例为}昆合性通气功能障碍伴弥散功能减低,2例为阻塞性通气功能障碍伴弥散功能减低。22例合并有肺动脉高压。肺间质病变在影像学上可有结节影、索条影、斑片影、网格影、磨玻璃影、肺大泡等多种改变。32例限制性通气功能障碍伴弥散功能减低患者中有15例表现为网格样、纤维化样改变,26例单纯弥散功能减低患者中有8例表现为网格样、纤维化样改变。结论结缔组织病肺间质病变患者呼吸系统表现多种多样,肺功能检查主要表现为限制性通气功能障碍伴弥散功能减低。混合性结缔组织病、重叠综合征、系统性红斑狼疮、系统性硬化症是较易出现肺间质病变合并肺动脉高压的结缔组织病。结缔组织病肺间质病变在影像学上可有多种多样改变,影像学上表现为网格样、纤维化样改变的患者肺功能易出现限制性通气伴弥散功能障碍。     

丙基硫氧嘧啶致肺血管炎1例报告及讨论

血管炎是丙基硫氧嘧啶的一种少见的药物不良反应，常累及皮肤和肾脏，肺部合并症罕见。本文报道的一例丙基硫氧嘧啶所致的抗中性粒细胞胞浆抗体(ANCA)阳性血管炎患者却仅有肺部受累表现，并在病程中出现呼吸衰竭。作者对其进行了纤维支气管镜及支气管透壁肺活检等检查。该例患者血中和支气管肺泡灌洗液中均检测到ANCA阳性，且非常见抗原类型，作者又对其抗原特异性进一步进行了分析。经停药并加用糖皮质激素治疗后，该患者症状完全消失。     

Does high-dose buprenorphine cause respiratory depression?: possible mechanisms and therapeutic consequences

Buprenorphine is an opioid agonist-antagonist with a 'ceiling effect' for respiratory depression. Compared with methadone, its unique pharmacology offers practical advantages and enhanced safety when prescribed as recommended and supervised by a physician. Buprenorphine has been approved in several countries as an efficient and safe maintenance therapy for heroin addiction. Its use resulted in a salutary effect with a reduction in heroin overdose-related deaths in countries that implemented office-based buprenorphine maintenance. In France, however, where high-dose buprenorphine has been marketed since 1996, several cases of asphyxic deaths were reported among addicts treated with buprenorphine. Death resulted from buprenorphine intravenous misuse or concomitant sedative drug ingestion, such as benzodiazepines. In these situations of abuse, misuse, or in association with elevated doses of psychotropic drugs, buprenorphine may cause severe respiratory depression. Unlike other opiates, the respiratory effects from buprenorphine are not responsive to naloxone. However, the exact mechanism of buprenorphine-induced effects on ventilation is still unknown. The role of norbuprenorphine, the main N-dealkylated buprenorphine metabolite with potent respiratory depressor activity, also remains unclear. Experimental studies investigating the respiratory effects of combinations of high doses of buprenorphine and benzodiazepines suggested that this drug-drug interaction may result from a pharmacodynamic interaction. A pharmacokinetic interaction between buprenorphine and flunitrazepam is also considered. As there are many questions regarding the possible dangers of death or respiratory depression associated with buprenorphine use, we aimed to present a comprehensive critical review of the published clinical and experimental studies on buprenorphine respiratory effects.     

肺部超声联合血清环状 RNA锚蛋白重复结构域 36评估新生儿急性呼吸窘迫综合征治疗效果和严重程度的价值

目的探讨肺部超声( LUS)、血清环状 RNA锚蛋白重复结构域 36(circANKRD36)水平在新生儿急性呼吸窘迫综合征(NRDS)疾病严重程度及治疗效果中的评估价值。方法选择郑州大学附属郑州中心医院 2020年 1月至 2022年 4月治疗的 109例 NRDS病儿为研究对象,根据氧合指数( OI)分为重度组( 48例)中度组( 35例)和轻度组( 26例);根据是否需要使用肺表面活性物质( PS)替代治疗分为对照组( 29例)和观察组( 80例)。收集病、儿资料,并对所有病儿治疗前、治疗后 12 h、治疗后 24 h、治疗后 72 h进行 LUS检查,采用实时荧光定量逆转录聚合酶链反应( qRT-PCR)法检测病儿各时间点血清 circANKRD36水平;绘制受试者操作特征曲线( ROC曲线)分析 LUS评分及血清 circANKRD36水平对 NRDS病儿疾病严重程度的评估价值。结果轻度组、中度组、重度组治疗前 LUS评,分及血清 circANKRD36水平依次升高( P<0.05)。以轻度组为对照, LUS评分、血清 circANKRD36水平及二者联合评估中度 NRDS的曲线下面积( AUC)分别为 0.81、0.70、0.86;以中度组为对照,各指标评估重度 NRDS的 AUC分别为 0.81、0.76、0.86。观察组治疗前肺实变、胸膜线异常、肺泡间质综合征、支气管充气征、胸腔积液比例均高于对照组( P<0.05)。观察组治疗前、治疗后 12 h、治疗后 24 h的 LUS评分及血清 circANKRD36水平均高于对照组( P<0.05)。经重复测量方差分析,两组 LUS评分及血清 circANKRD36水平在组间、时间、组间和时间存在交互效应( P<0.05),且观察组随治疗时间延长, LUS评分及血清 circANKRD36水平依次降低(P<0.05)。观察组总有效率为 95.00%(76/80),显著高于对照组的总有效率 72.41%(21/29)(P<0.05)。观察组治疗后 72 h肺实变、胸膜线异常、肺泡间质综合征、支气管充气征、胸腔积液比例显著低于治疗前( P<0.05)。结论 LUS评分及血清 circANKRD36水平可评估 NRDS病儿疾病严重程度,且二者联合的评估价值更高,同时可实时监测病儿治疗效果。